One of the quantitatively major inhibitory neurotransmitter substances present in the central nervous system is γ-amino butyric acid (GABA).i It exerts its physiological effect through three different receptor types, the ligand gated chloride channels GABAA and GABAC and the G-protein coupled GABAB receptor.ii The GABAA receptor complex is a pentameric assembly of several different protein subunits, which exist in multiple isoforms (α1-6, β1-4, γ1-4, θ, π, ε, ρ1-3 and δ).iii The most abundant of these GABAA receptors contain two α, two β and one γ subunits. Several ligands are known to allosterically modulate the GABAA receptor, such as benzodiazepine (BZD), barbiturates, ethanol and certain steroids.i 
Historically, the BZD has attracted most attention and has as such been used clinically for treatment as anxiolytic, anticonvulsant, muscle relaxant and sedative-hypnotic drugs.iv Among the wide variety of nonbenzodiazepine ligands, the most potent and perhaps best studied belong to the following classes: 2-arylpyrazoloquinolines, β-carbolines, pyridodiindoles, pyrimidin-5(6H)-ones, triazoloqunioxalines, cyclopyrrolones, and quinolines. The pharmacological effect of subtype-selective substances has been studied with the use of transgenic mice. Recent studies clearly suggest that a particular pharmacological response is associated with an action at a receptor with a specific subtype composition e.g. α1-containing receptors are involved in sedation and anterograde amnesia, and α2-, and/or α3- in anxiolytic activity, and α5-containing receptors might be associated with cognition and memory.v,vi It is believed that the BZD receptor is situated between the α- and γ-subunits, and a pharmacophore model of the binding site has been created. The model has later been refined through a SAR study of synthetical flavones, which added additional pharmacophore elements to the model.vii,viii 